White crystalline powder
(24S)-5,22-Stigmastadien-3b-ol/Stigmasta-5,22-dien-3-ol, (3β,22E)-/STIGMASTEROL (STIGMASTERIN)/(24S)-Stigmast-5,22-dien-3β-ol/STIGMASTEROL(P)/Wulzen anti-stiffness factor/Guinea-pig-anti-stiffness factor/SULFISOXAZOLE/Stigmasta-5,22-dien-3-ol, (3β,22E)- (9CI)/Stigmasta-5,22-dien-3β-ol/Stigmasterol/δ5,22-Stigmastadien-3β-ol/Anti-stiffness factor/(3β,22E)-Stigmasta-5,22-dien-3-ol/Stigmasta-5,22-dien-3-ol, (3β)-/Stigmasta-5,22-dien-3-ol, (3β,20R,22E,24S)-/Stigmasta-5,22-dien-3β-ol (8CI)/Stigmasta-5,22E-dien-3β-ol/isofucosterol/stigmasta-5,22-dien-3-b-ol/Stigmastero/STIGMASTA-5,22-DIEN-3-OL,(3B,22E)-/Stigmasterin/(3S,8S,9S,10R,13R,14S,17R)-17-[(2R,3E,5S)-5-Ethyl-6-methyl-3-hepten-2-yl]-10,13-dimethyl-2,3,4,7,8,9,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-3-ol/(3β,20R,22E,24S)-Stigmasta-5,22-dien-3-ol/3b-Hydroxy-24-ethyl-D5,22-cholestadiene/δ5-Stigmasterol/24S-ethylcholest-5,22-dien-3β-ol/stigmasta-5,22-dien-3-β-ol/β-Stigmasterol/(24S)-5,22-Stigmastadien-3β-ol/(3b,22E)-Stigmasta-5,22-dien-3-ol/5,22-stigmastadien-3β-ol/(3S,8S,9S,10R,13R,14S,17R)-17-[(2R,3E,5S)-5-ethyl-6-methylhept-3-en-2-yl]-10,13-dimethyl-2,3,4,7,8,9,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-3-ol/PHYTOSTEROL/(24S)-24-Ethylcholesta-5,22-dien-3β-ol
Stigmasterol is a plant sterol which has been focused on the cholesterol-lowering activity and is valued as an anti-stiffness factor in the therapy of rheumatic diseases.
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The therapeutic potential of stigmasterol, a natural steroid alcohol with established immune-modulatory properties, was assessed on allergic cutaneous responses. We examined its suppressive effect on immunoglobulin E (IgE)-mediated active cutaneous anaphylaxis (ACA), compound 48/80 (C48/80)-induced pruritus, and irritant dermatitis induced by 12-O-tetradecanoylphorbol-13-acetate (TPA). Stigmasterol at 10-100 mg/kg significantly inhibited ACA with reduction in reaction area and concentration of the extravasated Evans blue dye. Given at 50 and 100 mg/kg, stigmasterol significantly inhibited C48/80-induced scratching behaviour when compared to saline-treated C48/80-injected control. Skin histopathology of injected sites confirmed that stigmasterol reduced mast cell trafficking and degranulation associated with C48/80-induced pruritus. Stigmasterol controlled inflammatory features such as ear skin oedema and neutrophilia and also reduced serum levels of TNFα induced by topical application of TPA. Epidermal layer thickening and inflammatory cell infiltration of ear skin tissue were significantly reduced by stigmasterol. Taken together, stigmasterol demonstrates significant potential as a molecule of interest in allergic skin disease therapy.
Stigmasterol Alleviates Cutaneous Allergic Responses in Rodents.
Antwi AO1, Obiri DD1, Osafo N1, Essel LB1, Forkuo AD1, Atobiga C2.
2018 Jul 24
Stigmasterol is a phytosterol contained in Kraft mill effluent that is able to increase over 100% after aerobic biological treatment. This compound can act as an endocrine disrupter as its structure is similar to that of cholesterol. Furthermore, stigmasterol contained in Kraft mill effluent shows high toxicity (25-fold that of β-sitosterol) to aquatic organisms such as Daphnia magna (24-48 h). However, the operation of the aerobic treatment and biomass adaptation could be affecting their removal. The performances of activated sludge (AS), aerated lagoon (AL), and moving bed biofilm reactors (MBBR) are compared for removing stigmasterol contained in Kraft mill effluent. The AL operates at a hydraulic retention time of 6 h and removes up to 90% of phytosterols. So, a 96% of stigmasterol is removed by AL when the sterol retention load is 0.6 mg/L/day. However, stigmasterol concentrations increase from 29% to 37% at a low stigmasterol load rate (0.2 mg/L/day). On the other hand, the stigmasterol is removed between 65% and 87% by an AS under a hydraulic retention time of 3 h. Moreover, a 100% of stigmasterol can be removed by the MBBR when the hydraulic retention time is 2 days.
Activated sludge; Aerated lagoon; Kraft mill effluent; Moving bed biofilm reactors; Stigmasterol removal
Stigmasterol Removal by an Aerobic Treatment System.
Chamorro S1, Xavier C1,2, Hernandez V3, Becerra J3, Vidal G4.
To investigate and compare the effects of two common dietary phytosterols, stigmasterol and β-sitosterol, in altering lipid metabolism and attenuating nonalcoholic fatty liver disease (NAFLD).
Stigmasterol and β-sitosterol were administered to mice at 0.4% in a high-fat western-style diet (HFWD) for 17 weeks.
Stigmasterol and β-sitosterol significantly ameliorated HFWD-induced fatty liver and metabolic abnormalities, including elevated levels of hepatic total lipids, triacylglycerols, cholesterol and liver histopathology. Both phytosterols decreased the levels of intestinal bile acids, accompanied by markedly increased fecal lipid levels. In addition, they altered the expression of genes involved in lipid metabolism. β-Sitosterol was less effective in affecting most of these parameters. Lipidomic analysis of liver and serum samples showed that stigmasterol prevented the HFWD-induced elevation of some di- and triacylglycerol species and lowering of some phospholipid species. Stigmasterol also decreased serum levels of ceramides.
Stigmasterol and β-sitosterol, at a dose corresponding to that suggested for humans by the FDA for lowering cholesterol levels, are shown to alleviate HFWD-induced NAFLD. Stigmasterol was more effective than β-sitosterol, possibly because of its suppression of hepatic lipogenic gene expression and modulation of circulating ceramide levels.
Copyright © 2018 Elsevier B.V. All rights reserved.
Cholesterol; Fatty liver; Lipidomics; Mice; Stigmasterol; β-Sitosterol
Intake of stigmasterol and β-sitosterol alters lipid metabolism and alleviates NAFLD in mice fed a high-fat western-style diet.
Feng S1, Dai Z2, Liu AB3, Huang J4, Narsipur N3, Guo G5, Kong B5, Reuhl K5, Lu W6, Luo Z7, Yang CS8.